Scientists have a promising¹ new approach to combating deadly human viruses thanks to an educated hunch²（预感，肉峰） by University of California, Riverside microbiology professor Shou-Wei Ding, and his 20 years of research on plants, fruit flies, nematodes（线虫） and mice to show the truth in his theory. Researchers led by Ding, who heads a lab in UC Riverside's Institute for Integrative Genome Biology, have discovered that, like plants and invertebrate³（无脊椎的） animals, mammals use the RNA interference (RNAi) process to destroy viruses within their own cells.

 

Their findings will be published in the Oct. 11 issue of the journal Science.

 

Until now, scientists were unable to prove that mammals use RNAi for killing⁴ viruses, but ironically, it was Ding's earlier research into plants, nematodes and fruit flies that helped him find the key: viruses have been outwitting that innate⁵ protection in our cells by using proteins to suppress our virus-killing mechanism⁶.

 

Remove the suppressor protein from the virus, Ding's research discovered, and the subject's body will quickly eliminate the virus using the RNAi process, which sends out small interfering⁷ RNAs (siRNAs) to kill the disease.

 

In their research on young mice, for instance, all the subjects died when they were infected with the Nodamura virus, but when Ding's researchers removed the suppressor protein called B2 from the virus, the infected mice began producing huge armies of the virus-attacking siRNAs and lived, unaffected by the otherwise lethal⁸ infection.

 

"Many have tried to do this, that is, find the viral siRNAs in mammals, but they could not find the key," said Ding. "The key was our prior knowledge of the B2 protein in the Nodamura virus, a virus few people know about. Other scientists asked me, 'What is the Nodamura virus?' They have been studying the more well-known human viruses, but Nodamura virus infection of mice proves to be the best model."

 

How did Ding know where to look? The China native was partly acting⁹ on a hunch that started when he was a graduate student at the Australia National University in the late 1980s. There, during a lecture, he learned that the genomes of viruses infecting plants and animals are actually very similar, even though plants and animals are very different.

 

That, and further discussions with his mentor¹⁰ Adrian Gibbs, an expert on molecular¹¹ evolution of viruses and a fellow of the Australian Academy of Sciences, "made me think there must be a common anti-viral mechanism in plants and animals to keep their viruses similar," he said.

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